title: Cerebral metabolism after forced or voluntary physical exercise.
abstract: The pathophysiology of stroke, a leading cause of morbidity and mortality, is still in the process of being understood. Pre-ischemic exercise has been known to be beneficial in reducing the severity of stroke-induced brain injury in animal models. Forced exercise with a stressful component, rather than voluntary exercise, was better able to induce neuroprotection. This study further determined the changes in cerebral metabolism resulting from the two methods of exercise (forced versus voluntary). Adult male Sprague-Dawley rats were randomly assigned to 3 groups: the control group (no exercise), the forced treadmill exercise group, and the voluntary running wheel exercise group. In order to measure the extent of cerebral metabolism in animals with different exercise regimens, mRNA levels and protein expression of glucose transporter 1 and glucose transporter 3 (GLUT-1 and GLUT-3), phosphofructokinase (PFK), lactate dehydrogenase (LDH), and adenosine monophosphate kinase (AMPK) were measured utilizing real-time reverse transcription polymerase chain reaction (PCR) analysis as well as Western blot analysis. Phosphorylated AMPK activity was also measured using an ELISA activity kit, and hypoxic inducible factor (HIF)-1α was measured at transcription and translation levels. The data show that the forced exercise group had a significant (p < 0.05) increase in cerebral glycolysis, including expressions of GLUT-1, GLUT-3, PFK, LDH, phosphorylated AMPK activity and HIF-1α, when compared to the voluntary exercise and the control groups. Our results suggest that the effects of different exercise on HIF-1α expression and cerebral glycolysis may provide a possible reason for the discrepancy in neuroprotection, with forced exercise faring better than voluntary exercise through increased cerebral metabolism.
authors.affiliation: Department of Neurosurgery, Wayne State University School of Medicine, Detroit, MI, USA.
authors.forename: Harish
authors.initials: H
authors.lastname: Kinni
authors.forename: Miao
authors.initials: M
authors.lastname: Guo
authors.forename: Jamie Y
authors.initials: JY
authors.lastname: Ding
authors.forename: Sanjay
authors.initials: S
authors.lastname: Konakondla
authors.forename: David
authors.initials: D
authors.lastname: Dornbos
authors.forename: Raymond
authors.initials: R
authors.lastname: Tran
authors.forename: Murali
authors.initials: M
authors.lastname: Guthikonda
authors.forename: Yuchuan
authors.initials: Y
authors.lastname: Ding
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002540:Cerebral Cortex / Q000378:metabolism*; D051272:Glucose Transporter Type 1 / Q000096:biosynthesis; D051274:Glucose Transporter Type 3 / Q000096:biosynthesis; D006019:Glycolysis / Q000502:physiology; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000096:biosynthesis; D007770:L-Lactate Dehydrogenase / Q000096:biosynthesis; D008297:Male; D025221:Phosphofructokinases / Q000096:biosynthesis; D010805:Physical Conditioning, Animal / Q000379:methods*; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D051272:Glucose Transporter Type 1; D051274:Glucose Transporter Type 3; C497443:Hif1a protein, mouse; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D012333:RNA, Messenger; D007770:L-Lactate Dehydrogenase; D025221:Phosphofructokinases